Nickel substitution for calcium and the time course of potassium contractures of single muscle fibres.
In the virtual absence of external calcium (10(-9) M), peak tension of potassium contractures is not affected but their time course is markedly reduced. At 22 degrees C, the tension-time integral (area) of K+-contractures is reduced to about half its normal value. A similar reduction in the area of K+-contractures is observed when [Ca2+]0 is reduced to about 100 muM or less. When nickel substitutes for external calcium, K+-contractures present a normal time-course. Since nickel has been shown not to interact with contractile proteins these results indicate that extracellular calcium is apparently not directly participating in contractile activation nor in sustaining the time course of K+-contractures. External calcium deprivation affects also other phenomena related to excitation contraction coupling (ECC), such as the isometric tension-voltage relationship, the time course and extent of contractile repriming after a test contracture, the steady-state inactivation curve, and the capacity to sustain multiple contractures. Some of these effects indicate that external calcium may have a regulatory role on ECC phenomena. Nickel is an effective substitute for calcium in all these phenomena. The numerous contractures that a fibre can develop in the absence of calcium (nickel-substituted) indicate that the sarcoplasmic reticulum has either a large store of contractile activator, or a large recycling capacity.
D000663:Amphibians; D000818:Animals; D002118:Calcium / Q000494:pharmacology*; D004533:Egtazic Acid / Q000494:pharmacology; D007700:Kinetics; D009119:Muscle Contraction / Q000187:drug effects*; D009132:Muscles / Q000502:physiology; D009532:Nickel / Q000494:pharmacology*; D011188:Potassium / Q000378:metabolism*; D011894:Rana pipiens
D004533:Egtazic Acid; D009532:Nickel; D011188:Potassium; D002118:Calcium